Abstract

The photosystem II PsbS protein of thylakoid membranes is responsible for regulating the energy-dependent, non-photochemical quenching of excess chlorophyll excited states as a short-term mechanism for protection against high light (HL) stress. However, the role of PsbS protein in long-term HL acclimation processes remains poorly understood. Here we investigate the role of PsbS protein during long-term HL acclimation processes in wild-type (WT) and npq4-1 mutants of Arabidopsis which lack the PsbS protein. During long-term HL illumination, photosystem II photochemical efficiency initially dropped, followed by a recovery of electron transport and photochemical quenching (qL) in WT, but not in npq4-1 mutants. In addition, we observed a reduction in light-harvesting antenna size during HL treatment that ceased after HL treatment in WT, but not in npq4-1 mutants. When plants were adapted to HL, more reactive oxygen species (ROS) were accumulated in npq4-1 mutants compared to WT. Gene expression studies indicated that npq4-1 mutants failed to express genes involved in plastoquinone biosynthesis. These results suggest that the PsbS protein regulates recovery processes such as electron transport and qL during long-term HL acclimation by maintaining plastoquinone biosynthetic gene expression and enhancing ROS homeostasis.

Highlights

  • IntroductionPlants have developed sophisticated acclimation mechanisms to cope with unpredictable challenges in their environment

  • Being sessile organisms, plants have developed sophisticated acclimation mechanisms to cope with unpredictable challenges in their environment

  • To monitor the changes in PSII photochemical efficiency (Fv/Fm) of plant leaves under high light (HL) illumination, leaves of Arabidopsis WT and npq4-1 mutants grown at low (70 μmol photons m−2 s−1) photosynthetic photon flux density (PPFD) and were harvested in the middle of the day followed by exposure to HL at 700 μmol photons m−2 s−1 for up to five days

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Summary

Introduction

Plants have developed sophisticated acclimation mechanisms to cope with unpredictable challenges in their environment. When plants are exposed to excessive HL, the over-excitation of the photosynthetic apparatus triggers short-term protection mechanisms as well as several long-term acclimation processes. As an important short-term HL protection mechanism, non-photochemical quenching (NPQ) dissipates excess excitation energy as heat to reduce oxidative damage [1,2]. HL stress causes the generation of multiple reactive oxygen species (ROS), including hydrogen peroxide (H2O2), superoxide anion radicals (hereafter superoxide) (O2−), and singlet oxygen (1O2) that can cause damage and act as signaling molecules involved in regulating development and pathogen defense responses [9] The long-term protection mechanisms to HL stress or HL acclimation processes include dynamic changes in gene expression involved in hormone biosynthesis, signaling, and photosynthesis, the anthocyanin biosynthesis pathway genes [10], the composition, and the structure of the thylakoid membrane [11–14], accumulation of antioxidant metabolites and scavenging enzymes [15,16], and reducing LHCII antenna size [17–19]

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